VENTRICULAR ARRHYTHMIAS FOLLOWING ONE-STAGE AND 2-STAGE CORONARY REPERFUSION - EVIDENCE FOR BOTH REENTRY AND ENHANCED AUTOMATICITY
VENTRICULAR ARRHYTHMIAS FOLLOWING ONE-STAGE AND 2-STAGE CORONARY REPERFUSION - EVIDENCE FOR BOTH REENTRY AND ENHANCED AUTOMATICITY
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DOI：
10.1016/s0022-0736(85)80039-x
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发表时间：
1985-01-01
影响因子：
1.3
通讯作者：
LAZZARA, R
中科院分区：
文献类型：
--
作者：
KABELL, G;SCHERLAG, BJ;LAZZARA, R
用心电图和复合电图记录法研究了60条犬冠状动脉左前降支闭塞30-45分钟后再灌注的效果。15只犬中有14只在一段时间内再灌注产生室性心律失常，并在60 s内退化为室颤。室性心律失常的发生与再灌注区记录的心外膜和壁内电描记图中的连续电活动相关。再灌注期间迷走神经减慢（64 . ±. 8次/min）并不能预防室颤（8/8只犬），逸搏后通常伴随1次或多次与连续电活动相关的偶联异位搏动。快速心房起搏（270/min）也不能预防室性心律失常伴持续电活动和室颤的出现（6/6只犬），4 mg/kg利多卡因也不能预防（15/16只犬）。在另一组的15只狗再灌注进行了2个阶段，导致没有心室颤动，但在8 15只狗观察到室性心律失常开始在2分钟内再灌注后，持续20-30分钟。这些室性心律失常与连续的电活动在任何记录的铅。心房起搏可抑制室性心律失常，心室自主率平均为157。±-。10/min vs. 55 . ±. 10/min再灌注前对照。最早的激活部位表明自动灶出现在再灌注区的内膜下。利多卡因（2-4 mg/kg）迅速（< 90秒）恢复正常窦性心律并抑制自律性（72 ± 0.01）。左前降支再闭塞（52 ± 11/min）。6/min）。折返和增强的自律性在再灌注引起的室性心律失常中起作用。利多卡因（2-4 mg/kg）在该实验环境中抑制自主性但非折返性室性心律失常。
The effects of reperfusion were studied in 60 dogs following a 30-45 min period of left anterior descending coronary artery occlusion using ECG and composite electrogram recordings. One-stage reperfusion in 14 of 15 dogs produced ventricular arrhythmias which degenerated into ventricular fibrillation within 60 s. The onset of ventricular arrhythmias was associated with continuous electrical activity in epicardial and intramural electrograms recorded from the reperfused zone. Vagal slowing during reperfusion (64 .+-. 8/min) did not prevent ventricular fibrillation (8 of 8 dogs) and escape beats were often followed by 1 or more coupled ectopic beats associated with continuous electrical activity. Rapid atrial pacing (270/min) also did not prevent the appearance of ventricular arrhythmia with associated continuous electrical activity and ventricular fibrillation (6 of 6 dogs) nor did 4 mg/kg lidocaine (15 of 16 dogs). In another group of 15 dogs reperfusion was performed in 2 stages resulting in no ventricular fibrillation but in 8 of 15 dogs ventricular arrhythmias were observed beginning within 2 min after reperfusion and lasting 20-30 min. These ventricular arrhythmias were not associated with continuous electrical activity in any of the recorded leads. Atrial pacing suppressed ventricular arrhythmias and idioventricular rate averaged 157 .+-. 10/min vs. 55 .+-. 10/min pre-reperfusion control. The earliest site of activation indicated automatic foci arising in the subendocardium of the reperfused zone. Lidocaine (2-4 mg/kg) rapidly (< 90 s) restored normal sinus rhythm and suppressed automaticity (72 .+-. 11/min) as did left anterior descending artery reocclusion (52 .+-. 6/min). Reentry and enhanced automaticity play a role in ventricular arrhythmias due to reperfusion. Lidocaine (2-4 mg/kg) suppresses automatic but not reentrant ventricular arrhythmias in this experimental setting.